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. 2015 May;56(5):972–985. doi: 10.1194/jlr.M054635

Fig. 4.

Fig. 4.

Cholesterol efflux through the SR-BI pathway. A: Cholesterol efflux from BHK-SR-BI cells to the cholesterol acceptors of interest when SR-BI is not expressed (no mifepristone) or when SR-BI is expressed (10 nM mifepristone). B: SR-BI-specific cholesterol efflux was obtained by subtracting the average percent of unmediated (i.e., in the absence of mifepristone) efflux from individual cholesterol efflux values in cells expressing SR-BI. C: Specificity of BLT-1 and probucol inhibitory activity. BLT-1 inhibited SR-BI-mediated efflux in BHK-SR-BI cells, but did not inhibit the ABCG1 pathway in BHK-ABCG1 cells. Probucol affected neither the SR-BI- nor the ABCG1-mediated pathways in BHK-SR-BI and BHK-ABCG1 cells, respectively. D: Cholesterol efflux from Fu5AH cells with and without 1 μM BLT-1. The same amounts of the acceptors were added as in (A). E: SR-BI-specific cholesterol efflux from Fu5AH cells was obtained by subtracting the average percent of cholesterol efflux in the presence of BLT-1 from the corresponding individual cholesterol efflux values in vehicle-treated cells. Greater inhibition of cholesterol efflux with BLT-1 indicates a more robustly functioning SR-BI pathway. Values are mean ± SEM; n = 9 for BHK-SR-BI cells; n = 6 for Fu5AH cells. ***P < 0.001; *P < 0.1; ns, not significant.